Vishwa Deep Dixit, D.V.M., Ph.D.

Professor of Comparative Medicine and of Immunobiology
Yale School of Medicine

Vishwa Deep Dixit is a professor of comparative medicine and immunobiology at the Yale School of Medicine. He did Ph.D. research at University of Hannover, Germany, and postdoctoral research at the National Institutes of Health (NIH). Before joining Yale, he was a faculty member at the Pennington Biomedical Research Center, Baton Rouge.

Dixit’s research is focused on immunometabolism, with the goal to reveal molecular targets that can be harnessed to control inflammation and immune dysfunction as a means to enhance the healthspan. He has discovered that prolongevity hormone FGF21 protects against thymic degeneration in aging and T-cell senescence. His lab has helped define the role of innate immune sensor NLRP3 inflammasome in aging, insulin resistance, type 2 diabetes and immune senescence. His lab identified that ketone metabolite beta-hydroxybutyrate deactivates the NLRP3 inflammasome and thus serves as a therapeutic target to lower the NLRP3 inflammasome-dependent inflammatory diseases.

His work has been published in prominent journals, including Nature Immunology, Nature Medicine, Cell Metabolism, Cell Reports, PNAS and Journal of Clinical Investigation. He has received numerous awards for his research, including the Fellows Award for Research Excellence by NIH (thrice), Nathan Shock Young Investigator Awards from National Institute on Aging and Gerontological Society of America and the Young Investigator Award from the Endocrine Society. He received an honorary master of arts degree from Yale University in 2014. Dixit Laboratory is funded in part by NIH. 

Funded Research

Project Description Researchers Funding
Impact of Inflammasome Deactivation on Alzheimer’s Disease

This research proposal from the Dixit laboratory, which will be pursued in interdisciplinary collaboration with the lab of Dr. Rudy Tanzi at Massachusetts General Hospital (MGH), emanates from our original findings that NLRP3 inflammasome activation in microglia controls age-related inflammation in the central nervous system (CNS) and that CD33-dependent inhibition of amyloid-beta uptake by microglia reduces IL-1beta to protect against AD.

2016
$75,000